Abstract
The aim of the present study was to investigate the effect of ginsenoside compound K on β-amyloid (Aβ) peptide clearance in primary astrocytes. Aβ degradation in primary astrocytes was determined using an intracellular Aβ clearance assay. Aggregated LC3 in astrocyte cells, which is a marker for the level of autophagy, was detected using laser scanning confocal microscope. The effect of compound K on the mammalian target of rapamycin (mTOR)/autophagy pathway was determined using western blot analysis, and an enzyme-linked immunosorbent assay was used for Aβ detection. The results demonstrated that compound K promoted the clearance of Aβ and enhanced autophagy in primary astrocytes. In addition, it was found that phosphorylation of mTOR was inhibited by compound K, which may have contributed to the enhanced autophagy. In conclusion, compound K promotes Aβ clearance by enhancing autophagy via the mTOR signaling pathway in primary astrocytes.
Highlights
Alzheimer's disease (AD) is a progressive neurodegenerative disease of the central nervous system, with memory loss as the primary clinical manifestation
This indicates that compound K promotes Aβ clearance through the enhancement of autophagy in primary astrocytes
Compound K significantly reduced the expression level of P62 and the phosphorylation of ULK1, indicating that compound K activates and enhances autophagy in astrocytes. These results suggest that compound K may have an inhibitory effect on the phosphorylation of mammalian target of rapamycin (mTOR) and subsequently enhance autophagy, which may contribute to increased scavenging of Aβ in primary astrocytes
Summary
Alzheimer's disease (AD) is a progressive neurodegenerative disease of the central nervous system, with memory loss as the primary clinical manifestation. As a result of the aging population, the number of patients with AD is predicted to be >100 million in 2050 worldwide [1]. At present, there are no effective drugs that delay the progression of AD. Previous studies have demonstrated that β‐amyloid (Aβ) peptides have an important role in AD. Aggregation of Aβ may cause neurofibrillary tangles, inflammation and neuronal loss, resulting in the development of AD [2]. It is thought that reduced generation or accelerated clearance of Aβ may delay the pathological progression of AD [3,4].
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